Modern cardiac pacing systems have, in recent years, sought to incorporate at least some capability of detecting and dealing with various arrhythmias. For example, pacemaker designers have attempted to provide various special modes of pacing to control the effects of atrial and/or ventricular arrhythmias, particularly tachycardia and fibrillation. However, relatively little has been done to provide for preventive pacemaker therapy. For example, there is no known pacemaker therapy for preventing, or minimizing the risk of myocardia infarction (MI).
An early procedure adopted in pacemaker design for dealing with cardiac arrhythmias generally was simply to switch into an asynchronous mode, providing ordinary fixed rate asynchronous ventricular pacing. Such a response is a help, but is recognized to have limitations. Other more sophisticated response schemes have been adopted, with varying degrees of success. However, rather than simply trying to control the heart after the onset of a dangerous arrhythmia, it is to be recognized that it is preferable to anticipate when a patient may be potentially subject to a dangerous cardiac condition; and to take preventive action which aims to deal with the circumstances which give rise to the condition and thereby minimize its probability of occurrence. Relatively little work has been done in this area of preventive pacing therapies.
This invention is directed particularly toward preventing and/or responding to ventricular arrhythmias which have an increased incidence in the morning, after awakening. It is known from the literature that malignant arrhythmias, and types of acute myocardial infarctions, have a greater incidence in certain patients shortly after awakening. It is suggested that there is a circadian variability in the incidence of sudden cardiac death, with a peak in the early morning hours. See "Insights Into the Pathogenesis of Sudden Cardiac Death From Analysis of Circadian Fluctuations of Potential Triggering Factors," Hohnloser and Klingenheben, PACE, Vol. 17, March 1994, Part II, pp. 428-433. More specifically, as this reference indicates, there has been interest in exploring the relation between disturbances of ventricular repolarization, or prolonged QT interval, and sudden cardiac death. The distribution of occurences of MI over the 24-hour day reveals an increased risk shortly after the time of awakening and arising.
Other investigators likewise have discussed the potential correlation of such malignant arrhythmias and abnormal myocardial repolarization, or prolonged QT interval. It is known that the QT interval prolongs during sleep, and this prolongation extends into the arousal period. It is suggested that this QT interval prolongation may play an important role with respect to the diurnal variation of some ventricular arrhythmias. See, for example, "Prolongation of the Q-T Interval In Man During Sleep, "Browne et al,. The America Journal of Cardiology, July 1983, Vol. 52, pp. 55-59. See also "Electrocardiographic Repolarization During Stress From Awakening on Alarm Call," Tiovonen et al., JACC, Vol. 30, No. Sept. 3, 1997, pp. 774-779. It is known that the QT interval can vary independently of rate, and particularly that QT interval prolongs during sleep independent of any change of the RR interval. The cause of such QT variation, and the corresponding effect on cardiac rate stability, are the subject of considerable debate and analysis. However, there does appear to be a consensus that QT interval variability reaches a peak shortly after awakening, and that the time of this peak corresponds to the period of increased vulnerability to MI and ventricular tachycardias. Further, there is an inertia in adaptation of the QT interval during the period after awakening, i.e., the arousal period. By inertia it is meant that the QT interval does not directly shorten, but remains relatively prolonged, as patient heart rate increases during the time of arousal.
It is a basis of this invention that the delay in QT shortening, which results in a longer than normal QT interval after awakening, can result in an insufficient diastolic filling time for certain patients. Thus, if ventricular repolarization is extended relative to the patient's RR interval, the time available for diastolic filling is shortened. This in turn would lead to the result that insufficient blood is made available to flow through the myocardium, leaving the patient vulnerable to myocardial infarction.